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MS II Pharmacology Unit 1 > Cancer Pharmacology > Flashcards

Cancer Pharmacology Flashcards

1
Q

Principles of Chemo

A
  • use of chemical agents to kill or inhibit cancer cells
  • the ultimate goal of chemotherapy is a cure (long-term, disease-free survival); if a cure is not attainable, at least palliation (attenuation of symptoms)
  • chemotherapy is given to cancer patients whose neoplasms are not amenable to surgery or radiation therapy; also used as a supplemental treatment following surgery/radiation therapy to prevent metaastasis
  • most chemotherapeutic agents interfere with cell proliferation and/or induce apoptosis; rapidly dividing cancer cells are more sensitive to chemotherapy than normal cells
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2
Q

Log Kill Hypothesis

A
  • a given dose of drug kills a constant fraction of cells rather than a constant number of cells (first-order kinetics)
  • cell viability decreases with increased drug concentration
  • different drugs have different effects on cell viability
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3
Q

Principles of combination therapy

A
  • each drug used in the regiment should have individual anticancer actions
  • drugs that act by different mechanisms should be considered
  • the combination therapy should have additive or synergistic effects
  • drugs with different (non-overlapping) dose-limiting toxicities should be used
  • several cycles (6-8) of treatment should be given
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4
Q

Advantages of combination therapy

A
  • provide maximum cell killing with less toxicity
  • effective against heterogenous cell populations present in tumors
  • reduces the changes of development of resistant clones
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5
Q

Combination Regimens

A
  • ABVD- Hodgkin’s disease
  • CHOP- Non-Hodgkin’s lymphoma
  • MOPP- Hodgkin’s disease
  • CMF- Breast cancer
  • FEC- Breast cancer
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6
Q

Drug resistance

A
  • must tumors acquire drug resistance after prolonged administration of the drug
  • decreased cellular uptake
  • abnormal transport of the drug (rapid efflux by P-glycoprotein)
  • increased cellular inactivation (binding/metabolism)
  • altered target protein
  • reduced affinity for the drug
  • enhanced repair of DNA damage
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7
Q

Toxicity

A
  • chemotherapeutic agents aimed at killing cancer cells also affect normal cells undergoing rapid proliferation (eg BM, GI mucosa, hair follicles)
  • common side effects: neutropenia, thrombocytopenia, anemia, nausea, vomiting, stomatitis, alopecia (hair loss), leukemia/myelodysplasia in long term treatment with chemo agents
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8
Q

Cell cycle and anti-cancer drugs

A
  • cell cycle specific drugs (e.g. antimetabolites, vinca alkaloids)- active in a specific phase of the cell cycle, effective when a large proportion of tumor cells are proliferating (ie high growth fraction tumors); such as hematologic malignancies
  • cell cycle-nonspecific drugs (alkylating agents)- kill both cycling and noncycling tumor cells, effective against both low growth fraction tumors, such as solid tumors as well as high growth fraction tumors
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9
Q

Anticancer Drugs

A
  • alkylating agents
  • antimetabolites
  • DNA intercalating agents
  • microtubule inhibitors
  • topoisomerase inhibitors
  • hormones and their antagonists
  • miscellaneous agents (e.g. antibodies, kinase inhibitors)
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10
Q

Alkylating Agents Overview

A
  • compounds with the ability to transfer an alkyl group to DNA
  • promote cross-linking of DNA strands resulting in DNA damage
  • cell cycle non-specific agents- act on proliferating and resting cells
  • evolved from chemical warfare agents (mustard gas)
  • first agents use clinically to treat cancer patients; Goodman and Gilman initated clinical studies of nitrogen mustards in patients with lymphoma in 1942
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11
Q

Toxicities of Alkylating Agents

A
  • dose-related bone marrow suppression (neutropenia, thrombocytopenia, anemia)
  • mucosal toxicity (oral mucosal and GI ulceration)
  • nausea and vomiting
  • toxic effects on male and female reproductive system
  • highly carcinogenic; increased risk of secondary leukemia
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12
Q

Specific Alkylating Agents

A

1) Nitrogen Mustards- mechlorethamine, cyclophosphamide, ifosfamide
2) Nitrosoureas- Carmustine, Lomustine
3) Triazenes- Dacarbazine, Temozolomide
4) Platinum Analogs- Cisplatin, Carboplatin, Oxaliplatin

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13
Q

Mechlorethamine

A
  • nitrogen mustards
  • most reactive
  • first clinically used nitrogen mustard; used in combination reginmen MOPP
  • used topically for treatment of cutaneous T cell lymphoma
  • Toxicity: severe nausea and vomiting, myelosuppression
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14
Q

Cyclophosphamide/Ifosamide

A
  • nitrogen mustards
  • prodrugs that must be converted to active alkylating metabolites by P450
  • can be taken orally and they have a relatively long pasma half life
  • very broad clinical spectrum, component of many combination regimens (CHOP, CMF, FAC, FEC)
  • used for treatment of non-Hodgkin’s lymhoma, breast, lung and ovarian cancer
  • Ifosamide- sarcoma and testicular cancer
  • Toxicity: nausea, vomiting, myelosuppression
  • hemorrhagic cystitis (due to accumulation of toxic metabolite acrolein); administration of MESNA (2-mercaptoethane sulfonate) minimizes this problem
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15
Q

Nitrosoureas

A
  • type of alkylating agent

- Carmustine and Lomustine

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16
Q

Carmustine and Lomustine

A
  • nitrosoureas (alkylating agent)
  • therapeutic uses- they are highly lipophilic, used for treatment of meningeal leukemias and brain tumors
  • Toxicity- severe nausea and vomiting, profound myelosuppression, renal toxicity, pulmonary fibrosis
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17
Q

Triazenes

A
  • Dacarbazine and Temozoi

- pro-drugs, monoalkylators

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18
Q

Dacarbazine, Temozolomide

A
  • triazenes (type of alkylating agent)
  • pro-drugs
  • therapeutic uses- decarbazine is a compoent of ABVD regiment used for treatment of Hodgkin’s disease
  • Temozolomide has shown activity against malignant glioma
  • toxicity- nausea and vomiting, myelosuppression, flu-like symptoms
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19
Q

Platinum Analogs

A
  • Cisplatin, Carboplatin, oxaliplantin
  • inorganic platinum derivatives; covalently bind to nucleophilic sites (N7 of guanine) on DNA
  • form intrastrand and intersrand cross links
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20
Q

Cisplatin

A
  • Platinum Analogs
  • efficacy against a wide range of neoplasms
  • used for treatment of testicular, ovarian, cervical and bladder cancers
  • nephrotoxicity (renal tubular damage and necrosis); ototoxicity (hearing loss); peripheral neuropathy; nausea and vomiting; myelosuppression
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21
Q

Carboplatin

A
  • platinum analog
  • ovarian cancer
  • less toxic and less reactive
  • thrombocytopenia is dose-limiting
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22
Q

Oxaliplatin

A
  • platinum analog
  • used in combo with 5-FU for gastric and colorectal cancer
  • unique toxicity- cold-induced acute peripheral neuropathy
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23
Q

Antimetabolites

A
  • structural analogs of endogenous folates, purines and pyrimidines
  • inhibit enzymes required for nucleotide synthesis or complete with endogenous nucleotides in DNA or RNA synthesis
  • act specifically in the DNA synthesis (S) phase of the cell cycle; thus considered as cell cycle specific (ccs) drugs
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24
Q

Antimetabolite types

A

1) Folate Analogs- methotrexate, pemetrexed
2) Pyrimidine Analogs- 5-Flurouracil, Cytarabine, Gemcitabine
3) Purine Analogs- 6- Mercaptopurine

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25
Q

Folate Analogs

A
  • type of antimetabolite

- Methotrexate (MTX)

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26
Q

Methotrexate

A
  • most widely used antimetabolite in cancer chemotherapy
  • produced first striking remission of leukemia
  • produced first cure of solid tumor (choriocarcinoma)
  • inhibits the enzyme dihydrofolate reductase
  • effective in treating childhood ALL, choriocarcinoma, osteosarcoma, breast cancer, head and neck cancer
  • usually given orally; administered intrathecally for meningeal leukemia
  • toxicity- bone marrow toxicity (myelosuppression), GI toxicity (oral ulceration, stomatitis, renal toxicity (MTX can crystallize in the urine and cause renal damage), hepatotoxicity (long-term use of MTX may lead to fibrosis or cirrhosis
  • Mechanisms of Resistance- reduced drug uptake by neoplastic cells, increased production of DHPR (gene amplification), decreased affinity of DHFR for MTX
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27
Q

Pemetrexed

A
  • a multi-targeted folate analog, which inhibit both DHFR and thymidylate synthetase
  • approved fir treatment of non-small cell lung cancer and mesothelioma, colon and pancreatic
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28
Q

Leucovorin rescue

A
  • prevention of the toxic effects of MTX by Leucovorin
  • N-5 formyltetrahydrofolate) is administered to the patient several hours after an otherwise lethal dose of methotrexate
  • the malignant cells are killed selectively, while the normal cells are rescued by the folinic acid.
  • one hypothesis is that tumor cells cannot uptake folinic acid (Leucovorin) whereas normal cells can uptake folinic acid and bypass the requirement of DHFR
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29
Q

Pyrimidine Analogs

A
  • 5-Fluorouracil
  • Cytarabine
  • Gemcitabine
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30
Q

5-Fluorouracil (5-FU)

A
  • a pro-drug requiring enzymatic conversion into active metabolites 5-FdUMP) and (5-FdUTP) to exert its cytotoxic activity
  • 5-dUMP inhibits thymidylate synthase and prevents the synthesis of thymidine, a major building block of DNA
  • FdUTP is incorporated into RNA by RNA polymerase and interferes with RNA function
  • therapeutic uses- must be given IV due to rapid metabolic degradation in the gut and liver, used as a compnent of combo regiments for treatment of breast, colorectal, gastric, head and neck, cervical and pancreastic cancers, used topically for basal cell carinomas
  • toxicity- anorexia and nausea, mucosal ulcerations, stomatits and diarrhea, thrombocytopenia and anemia, hand-foot syndrome-erythema, senesitivity to the palms and soles, cardiac toxicity- acute chest pain
31
Q

Cytarabine (Ara-C)

A
  • type of pyrimidine analog
  • analog of 2’ deoxycytidine (natural ribose is replaced by D-arabinose)
  • converted to Ara-CMP by deoxycytidine kinase
  • Ara-CMP is subsequnetly converted to Ara-CTP, which competes swith dCTP for incorporation into DNA by DNA polymerase
  • when incorporated into DNA, Ara-CTP inhibits DNA synthesis
  • therapeutic uses- most effective for treatment of AML, also useful for ALL and blast phase CML
  • toxicity- severe myelosuppression
  • GI tract toxicity (ulceration, stomatits, diarrhea)
32
Q

Gemcitabine

A
  • type of pyrimidine analog
  • a difluoro analog of deoxycytidine (dFdC)
  • converted to active di- and tri- phosphate metabolites (dFdCDP, dFdCTP)
  • dFdCCP inhibits ribonucleotide reductase, resulting in the depletion of deoxyribonucleotides necessary for DNA synthesis
  • dFdCTP competes with dCTP for incorporation into DNA and leads to termination of DNA synthesis
  • more effective in treating solid tumors than cytarabine
  • therapeutic= used as a first-line treatment for pancreatic carcinoma, it is also effective against non-cell lung cancer, ovarian, bladder, esophageal and head and neck cancer
  • toxicity- myelosuppression (leukopenia, thrombocytopenia, anemia), flu-like syndrome
33
Q

Purine analogs

A
  • a treatment for hyperuricemia and gout
  • later purine analogs have been found useful for treatment of cancer
  • 6- Mercaptopurine
34
Q

6-Mercaptopurine

A
  • a pro-drug
  • requires enzymatic conversion to ribonucleotide by HGPRT
  • it causes a reduction in purine levels resulting in inhibition of DNA and RNA synthesis in tumor cells
  • it is prodrug that must be metabolized by HGPRT to the ribonucleotide-6-thioionsinic acid (TIMP)
  • TIMP inhibits the first step of the de novo synthesis of the purine base
  • TIMP also blocks formation of AMP and xanthinylic acid from inosinic acid
  • also TIMP is converted to thio guanine ribonucleotides, which are incorporated into DNA and RNA resulting in inhibition of DNA and RNA synthesis
  • therapeutic uses- used primarily to maintain remission in patients with ALL
  • Toxicity- bone marrow suppression, hepatotoxicity in prolonged use of 6-MP
  • Mechanism of Resistance- decreased expression of HGPRT, decreased drug transport
  • drug interaction with allopurinol- allopurinol inhibits xanthine oxidase and thereby increases plasma MP levels (you need to decrease the dose of 6-MP in patients receiving allopurinol to avoid accumulation of the drug and exacerbation of toxicities
35
Q

DNA Intercalating Agents

A
  • anti-tumor antibiotics
  • derived from various strains of Streptomyces
  • bind to DNA through intercalation between specific bases and block synthesis of DNA, RNA or both
  • cause DNA strands break and interfere with cell replication
36
Q

Dactinomycin

A
  • first anticancer antibiotic derived from Streptomyces
  • intercalates between adjacent G-C base pairs
  • interferes with DNA-dependent RNA polymerase, causing inhibition of DNA transcription
  • causes single strand breaj
  • used for treatment of rhabdomyosarcoma, Wilm’s tumor and Ewing’s sarcoma in children
  • toxicity: anorexia, nausea and vomiting, may cause hematopoietic suppression with pancytopenia
37
Q

Anthracyclins

A
  • DNA intercalating agents
  • Daunorubicin, Doxorubicin, Epirubicin, Idarubicin
  • they intercalate between DNA base pairs
  • anthracyclines are reduced to intermediates that donate electrons to oxygen to form superoxide
  • superoxide then reacts with itself to make hydrogen peroxide which is cleaved in the presence of iron to form the destructive hydroxyl radical that cleaves DNA
38
Q

Doxorubicin

A
  • also known as adriamycin
  • has broad clinical spectrum; one of the most widely used anticancer drugs
  • used for treatment of sarcomas, breast and lung carcinomas and lymphomas
  • toxicity- dose dependent cardiotoxicity (cardiomyopathy), neutropenia, stomatitis, alopecia
39
Q

Daunorubicin and Idarubicin, Epirubicin and Mitoxantrone

A
  • other anthracyclines
  • Daunorubicin and Idarubicin- used in combination with Ara-C for treatment of AML
  • Epirubicin- used in combo regimen for treatment of metastatic breast cancer
  • Mitoxantrone- less cardiotoxic than other anthracyclines, approved from treatment of AML and late stage multiple sclerosis
  • -toxicity- dose dependent cardiotoxicity (cardiomyopathy), neutropenia, stomatitis, alopecia
40
Q

Bleomycin

A
  • DNA intercalating Agent
  • mixture of two peptides obtained from streptomyces
  • binds to DNA, induces single and double stranded DNA breaks in the G2 phase of the cell cycle
  • therapeutic uses- used as a component of PEB combo regimen for treatment of testicular carcinomas or as a component of ABVD regimen for Hodgkin’s disease
  • also effective against squamous cell carcinomas
  • toxicity- severe dose-related pulmonary toxicity (pulmonary fibrosis), minimally myelosuppressive, cutaneous toxicity (hyperpigmentation, hyperkeratosis, erythema)
41
Q

Microtubule Inhibitors

A
  • plant natural products
  • bind tubulin, interfere with microtubule function
  • causes mitotic arrest (M phase of cell cylcle)
  • Vinca Alkaloids- Vinblastine, Vincristine
  • Taxanes- Paclitaxel, Docetaxel
42
Q

Vinca Alkaloids

A
  • derived from the periwinkle plant Vinca rosea

- bind to tubulin, and prevent polymerization of tubulin into microtubules

43
Q

Vinblastine

A
  • vinca alkaloid (microtubule inhibitor)
  • component of ABVD for Hodgkin’s lymphoma
  • toxicity- myelosuppression, nausea, vomiting
  • resistance- amplification of P-glycoprotein; mutations in tubulin resulting in reduced binding of the drugs to their target
44
Q

Vincristine

A
  • vinca alkaloid (microtubule inhibitor)
  • used with glucocorticoids in the treatment of childhood ALL; also a component of MOPP regimen for Hodgkin’s lymphoma
  • toxicity- dose-limiting neurotoxicity (peripheral neuropathy) but relatively low toxicity in the bone marrow
  • resistance- amplification of P-glycoprotein; mutations in tubulin resulting in reduced binding of the drugs of their target
45
Q

Taxanes

A
  • microtubule inhibitors
  • Paclitaxel and Docetaxel
  • alkaloids derived from the yew trees
  • Paclitaxel- bark, Docetaxel- needles
  • bind to to tubulin and prevent depolymerization of microtubules which is necessary from chromosome desegregation during mitosis
46
Q

Paclitaxel

A
  • microtubule inhibitor- taxane
  • components of regimen used for treatment of metastatic breast, ovarian, lung and head and neck cancers
  • toxicity- neutropenia, peripheral neuropathy, hypersensitivity reactions
47
Q

Docetaxel

A
  • components of regimen used for treatment of metastatic breast, ovarian, lung and head and neck cancers
  • useful against hormone- refractory prostate cancer
  • toxicity- neutropenia, peripheral neuropathy, hypersensitivity reactions
48
Q

Topoisomerase Inhibitors

A
  • topoisomerases mediate DNA strand breakage and resealing during replication or transcription of DNA
  • Top1 breaks and reseals single stranded DNA, whereas Top II breaks and reseals double stranded DNA
  • inhibitors of topoisomerases cause permanent DNA strand breaks by preventing the resealing of nicked strands of DNA
  • Epipodophyllotoxin- Etoposide, Teniposide
  • Camptothecin Analogs- Irinotecan, Topotecan
49
Q

Epipodophyllotoxins

A
  • Etoposide, Teniposide

- inhibit Top II

50
Q

Etoposide

A
  • Top II inhibitor, epipodophyllotoxin
  • broad clinical spectrum; used for treatment of testicular carcinoma, lung cancer, and non-Hodgkin;s lymphoma
  • toxicity- dose-limiting myelosuppression (neutropenia), oral mucositis
51
Q

Teniposide

A
  • Top II inhibitor, epipodophyllotoxin
  • mainly used for acute lymphoblastic leukemia ALL
  • toxicity- dose limiting myelosuppression (neutropenia), oral mucositis
52
Q

Camptothecin Analogs

A
  • irinotecan, topotecan

- inhibit Top I

53
Q

Irinotecan

A
  • inhibit Top I
  • camptothecin analog
  • approved for treatment of advanced colorectal cancer; also used for lung, ovarian, cervical and brain tumors
  • toxicity- severe neutropenia, severe diarrhea
54
Q

Topotecan

A
  • inhibit TopI
  • camptothecin analog
  • indicated for treatment of ovarian and small cell lung cancer
  • toxicity- severe neutropena, severe diarrhea
55
Q

When is hormonal therapy useful?

A
  • lymphomas and leukemia
  • breast cancer
  • prostate cancer
56
Q

Glucocorticoids

A
  • have shown cytotoxic effects on lymphocytes
  • they inhibit mitosis in lymphocytes
  • they are relatively well tolerated and do not induce myelosuppression
57
Q

Prednisone

A
  • glucocorticoids (inhibit mitosis in lymphocytes)
  • prednisone plus vincristine produce remission in patients with ALL
  • also a component of combination regiments (MOPP and CHOP) for Hodgkin’s and non-Hodgkin’s lymphomas
58
Q

Dexamethsaone

A
  • glucocorticoid (cytotoxic and inhibit mitosis in lymphocytes)
  • used to reduce edema following radiation therapy
59
Q

Hormone Therapy for Breast Cancer

A
  • breast cancer is usually estrogen dependent and can be suppressed by administration of estrogen antagonists
  • Selective Estrogen-Receptor Modulators (SERMs): Tamoxifen
  • Selective Estrogen-Receptor Down regulators (SERDs): Fulvestrant
  • Aromatase Inhibitors- Aminoglutethamide, Anastrozole, Letrozole, Exemestane
60
Q

Tamoxifen

A
  • competes with estradiol for binding to the ER, resulting in non-functional hormone receptor complex
  • used for treatment of ER- positive early stage and metastatic breast cancer
  • used for prevention of breast cancer in high risk patients (family history)
  • toxicity- hot flushes, hair loss, nausea and vomiting, weak agonist in endometrium; increased risk of endometrial cancer and thromboembolism
61
Q

Fulvestrant

A
  • first FDA approved SERD (Selective Estrogen-receptor downregulators)
  • binds to ER with a much higher affinity (>100 fold) than tamoxifen
  • reduces ER expression
  • approved for postmenopausel women with ER- positive metastatic breast cancer
62
Q

Aromatase Inhibitors

A
  • inhibit the enzyme aromatase, which is necessary for estrogen synthesis
  • Als cause profound estrogen deprivation in postmenopausal women
  • aminoglutethamide, Anastrozole, Letrozole, Exemestane
63
Q

Aminoglutethamide

A
  • aromatase inhibitors
  • a first generation Al; it has beneficial effects against breast cancer
  • has signficant toxicity; replaced by third generation Als
64
Q

Anastrozole, Letrozole, Exemestane

A
  • third generation Al; potent and selective inhibitor of aromatase
  • Anastrozole and Letrozole are non-steroidal reversible inhibitors of aromatase
  • Exemestate is a steroidal inhibitor of aromatase; it competes with the natural substrate androstenedione; irreversibly inactivates aromatase
  • 3rd generation- used for treatment of early and late stage breast cancer
  • have replaced tamoxifen as first-line therapy for postmenopausal ER+ breast cancer
65
Q

Hormone Therapy for Prostate Cancer

A
  • androgen deprivation therapy (ADT) through either surgical or medical castration is useful for treatment of advanced prostate cancer
  • Leuprolide, Goserelin
  • Flutamide, Bicalutamide
66
Q

Leuprolife, Goserelin

A
  • hormone for prostate cancer
  • are GnRH analogs
  • bind to GnRH receptor and inhibit the release of FSH and LH, resulting in reduced testicular production of testosterone
  • do not inhibit adrenal androgen synthesis
67
Q

Flutamide, Bicalutamide

A
  • hormone for prostate cancer
  • are non-steroidal androgen-receptor (AR) blockers
  • compete with natural hormone for binding with the AR
68
Q

Hydroxyurea

A
  • Misc cancer drug
  • inhibits ribonucleotide reductase, which catalyzes the conversion of ribonucleotides to deoxyribonucleotides
  • useful for treatment of MPDs (CML, PV, ET) and sickle cell disease
69
Q

Retinoids

A
  • all trans retinoic acid is very useful in the treatment of acute promyleocytic leukemia (APL)
  • it induces differentiation in leukemic promyleocytes and produces remission in patients with APL
70
Q

Arsenic Trioxide

A
  • misc agents

- a heavy metal toxin highly effective in the treatment of relapsed APL

71
Q

Thalidomide

A
  • misc agents
  • inhibits the production of IL-6, which is a growth factor for myeloma cells
  • inhibits TNFalpha signaling (immunodulatory effects)
  • exhibits antiangiogenic activity
  • activates the apoptotic pathways
  • approved for treatment of multiple myeloma
72
Q

Interferon-alpha

A

-approved for treatment of hairy cell leukemia, CML and AIDS-related Kaposi’s sarcoma

73
Q

Tyrosine Kinase Inhibitors

A
  • imatinib (Abl inhibitor) for treatment of CML, also inhibits PDGFR and c-kit
  • gefitinib/erlotinib *EGFR inhibitor) for treatment of non-small cell lung cancer
74
Q

Monoclonal Antibodies

A
  • Trastuzumab for treatment of metastatic HER2+ breast cancer
  • Cetuximab (a mAB against ErbB1) for treatment of metastatic colon cancer)

MS II Pharmacology Unit 1 (10 decks)

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